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  • Springer (CrossRef)  (28)
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  • 1
    Language: English
    In: Neurological Sciences, 2011, Vol.31(Supplement 3), pp.283-288
    Description: Monoclonal antibodies, first introduced in cancer therapy and to prevent allograft rejection, represent new pharmacological tools for the treatment of autoimmune diseases. With the knowledge of immunological movements in autoimmunity, it is now possible to target each single step of the immune process, from the activation of T lymphocytes in lymph nodes to the formation of the immunological synapse, and to T cell differentiation and cytokine production. However, this approach is still not devoid of adverse effects. In fact, even if monoclonal antibodies exert selective immunomodulation by targeting only cells expressing a specific antigen, a widespread perturbation of the immune system is induced, leading to a predisposition for infections and infestations and to the occurrence of tumours.
    Keywords: Biological drugs ; Monoclonal antibodies ; Autoimmune diseases ; Multiple sclerosis
    ISSN: 1590-1874
    E-ISSN: 1590-3478
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  • 2
    Language: English
    In: Diabetologia, 2014, Vol.57(5), pp.980-990
    Description: Byline: Ivana Nikolic (1), Tamara Saksida (1), Katia Mangano (2), Milica Vujicic (1), Ivana Stojanovic (1), Ferdinando Nicoletti (2), Stanislava Stosic-Grujicic (1) Keywords: Beta cell apoptosis; Carbon monoxide-releasing molecule-A1; Cytokines; Type 1 diabetes Abstract: Aims/hypothesis Recent studies have identified carbon monoxide (CO) as a potential therapeutic molecule for the treatment of autoimmune diseases owing to its anti-inflammatory and anti-apoptotic properties. We explored the efficacy and the mechanisms of action of the CO-releasing molecule (CORM)-A1 in preclinical models of type 1 diabetes. Methods The impact of CORM-A1 on diabetes development was evaluated in models of spontaneous diabetes in NOD mice and in diabetes induced in C57BL/6 mice by multiple low-dose streptozotocin (MLDS). Ex vivo analysis was performed to determine the impact of CORM-A1 both on T helper (Th) cell and macrophage differentiation and on their production of soluble mediators in peripheral tissues and in infiltrates of pancreatic islets. The potential effect of CORM-A1 on cytokine-induced apoptosis in pancreatic islets or beta cells was evaluated in vitro. Results CORM-A1 conferred protection from diabetes in MLDS-induced mice and reduced diabetes incidence in NOD mice as confirmed by preserved insulin secretion and improved histological signs of the disease. In MLDS-challenged mice, CORM-A1 attenuated Th1, Th17, and M1 macrophage response and facilitated Th2 cell differentiation. In addition, CORM-A1 treatment in NOD mice upregulated the regulatory arm of the immune response (M2 macrophages and FoxP3.sup.+ regulatory T cells). Importantly, CORM-A1 interfered with in vitro cytokine-induced beta cell apoptosis through the reduction of cytochrome c and caspase 3 levels. Conclusions/interpretation The ability of CORM-A1 to protect mice from developing type 1 diabetes provides a valuable proof of concept for the potential exploitation of controlled CO delivery in clinical settings for the treatment of autoimmune diabetes. Author Affiliation: (1) Department of Immunology, Institute for Biological Research 'Sinisa Stankovic', University of Belgrade, Bul. Despota Stefana 142, 11060, Belgrade, Serbia (2) Department of Biomedical Sciences, School of Medicine, University of Catania, Via Androne 83, 95124, Catania, Italy Article History: Registration Date: 10/01/2014 Received Date: 19/07/2013 Accepted Date: 18/12/2013 Online Date: 02/02/2014 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00125-014-3170-7) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
    Keywords: Beta cell apoptosis ; Carbon monoxide-releasing molecule-A1 ; Cytokines ; Type 1 diabetes
    ISSN: 0012-186X
    E-ISSN: 1432-0428
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  • 3
    Language: English
    In: Psychopharmacology, 2011, Vol.217(3), pp.301-313
    Description: Byline: Sara Morley-Fletcher (1), Jerome Mairesse (1), Amelie Soumier (2), Mounira Banasr (2), Francesca Fagioli (3), Cecilia Gabriel (4), Elisabeth Mocaer (4), Annie Daszuta (2), Bruce McEwen (5), Ferdinando Nicoletti (1,6,7), Stefania Maccari (1) Keywords: Agomelatine; Prenatal stress; Adult neurogenesis; Ventral hippocampus; Fluoxetine; Phospho-CREB; Metabotropic glutamate receptors Abstract: Rationale and objectives The rat model of prenatal restraint stress (PRS) replicates factors that are implicated in the etiology of anxious/depressive disorders. We used this model to test the therapeutic efficacy of agomelatine, a novel antidepressant that behaves as a mixed MT1/MT2 melatonin receptor agonist/5-HT.sub.2c serotonin receptor antagonist. Results Adult PRS rats showed behavioral, cellular, and biochemical abnormalities that were consistent with an anxious/depressive phenotype. These included an increased immobility in the forced swim test, an anxiety-like behavior in the elevated plus maze, reduced hippocampal levels of phosphorylated cAMP-responsive element binding protein (p-CREB), reduced hippocampal levels of mGlu2/3 and mGlu5 metabotropic glutamate receptors, and reduced neurogenesis in the ventral hippocampus, the specific portion of the hippocampus that encodes memories related to stress and emotions. All of these changes were reversed by a 3- or 6-week treatment with agomelatine (40--50 mg/kg, i.p., once a day). Remarkably, agomelatine had no effect in age-matched control rats, thereby behaving as a "disease-dependent" drug. Conclusions These data indicate that agomelatine did not act on individual symptoms but corrected all aspects of the pathological epigenetic programming triggered by PRS. Our findings strongly support the antidepressant activity of agomelatine and suggest that the drug impacts mechanisms that lie at the core of anxious/depressive disorders. Author Affiliation: (1) Neuroplasticity Team, UMR 8576 CNRS Structural and Functional Glycobiology Unit, University Lille North of France (USTL), 59655, Villeneuve d'Ascq, France (2) IC2N, IBDLM, UMR6216, CNRS, Marseille, France (3) Azienda Sanitaria Locale, RM.E. Unita Operativa Complessa Adolescent, Rome, Italy (4) Institut de Recherches Internationales Servier, Courbevoie, France (5) Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, USA (6) Department of Human Physiology and Pharmacology, Sapienza University, Rome, Italy (7) I.N.M. Neuromed, Pozzilli, Italy Article History: Registration Date: 24/03/2011 Received Date: 10/01/2011 Accepted Date: 23/03/2011 Online Date: 19/04/2011 Article note: S. Morley-Fletcher and J. Mairesse contributed equally to this work.
    Keywords: Agomelatine ; Prenatal stress ; Adult neurogenesis ; Ventral hippocampus ; Fluoxetine ; Phospho-CREB ; Metabotropic glutamate receptors
    ISSN: 0033-3158
    E-ISSN: 1432-2072
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  • 4
    Language: English
    In: European Child & Adolescent Psychiatry, 2017, Vol.26(12), pp.1433-1441
    Description: This study aims at determining serum levels of tryptophan and other metabolites of the kynurenine pathway in children with attention deficit hyperactivity disorder (ADHD) compared to healthy controls. Such metabolites interact with glutamate receptors in the central nervous system, potentially modulating mechanisms that are pivotal in ADHD and thus potentially representing peripheral biomarkers of the disorder. We measured serum levels of tryptophan and some metabolites of the kynurenine pathway in 102 children with ADHD and 62 healthy controls by liquid chromatography–tandem mass spectrometry (LC–MS/MS). As compared to healthy controls, children with ADHD showed a reduction in serum levels of anthranilic acid (−60%), kynurenic acid (−11.2%), and xanthurenic acid (−12.5%). In contrast, serum levels of tryptophan (+11.0%) and kynurenine (+48.6%) were significantly enhanced, and levels of quinolinic acid were unchanged in children with ADHD. In a logistic regression model, the presence of ADHD was predicted by low anthranilic acid and high tryptophan levels. These findings support the involvement of the kynurenine pathway in the pathophysiology of ADHD and suggest that anthranilic acid and tryptophan levels should be investigated as potential peripheral biomarker for ADHD.
    Keywords: ADHD ; Biomarker ; Kynurenines ; Children ; Neurobiology
    ISSN: 1018-8827
    E-ISSN: 1435-165X
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  • 5
    Language: English
    In: Immunologic Research, 2012, Vol.52(1), pp.157-168
    Description: Development of resistance to TRAIL-induced toxicity is one of the strategies used from tumor cells to escape destruction from the immune system. This process may occur through aberrant expression of functional receptors, overexpression of decoy receptors on tumor cell membrane, or malfunctioning of downstream signals triggered by specific ligation of TRAIL. Numerous cytostatic, but also noncytostatic, drugs like protease inhibitors and NO-hybridized molecules have been shown to revert sensitivity of neoplastic cells to TRAIL by means of different mechanisms. This paper will review the possible routes of reconstitution of sensitivity to TRAIL-mediated immune response by specific modulation of different signals responsible for the development of resistance at both the membrane and the intracellular levels. Moreover, we will review and suggest novel strategies, aimed at resetting immune cell efficiency in cancer treatment.
    Keywords: TRAIL resistance ; Death receptors ; Saquinavir-NO
    ISSN: 0257-277X
    E-ISSN: 1559-0755
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  • 6
    Language: English
    In: Neurology and Therapy, 01 November 2018, Vol.7(2), pp.385-390
    Keywords: Equivalence ; Follow-on Glatiramer Acetate ; Glatiramer Acetate ; Multiple Sclerosis
    ISSN: 2193-8253
    E-ISSN: 2193-6536
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  • 7
    Language: English
    In: Inflammation Research, 2012, Vol.61(10), pp.1131-1139
    Description: Objective: To evaluate the heat shock protein (HSP) variation during the differentiation and polarization of human macrophages. Methods: Gene expression analysis was investigated by real-time PCR from mRNA of human monocytes obtained from the buffy coats of healthy volunteers, polarized to classically activated macrophages (or M1), whose prototypical activating stimuli are interferon-gamma and lipopolysaccharide, and alternatively activated macrophages (or M2) obtained by interleukin-4 exposure. The modulation of HSPs at the transcriptomic levels was investigated using oligonucleotide microarray in the process of primary human monocyte-to-macrophage maturation and subsequent polarization into M1 or M2 cells. Results: We found that 11 HSPs transcripts were modulated throughout monocyte-to-macrophage differentiation. Furthermore a considerable effect on HSP expression was detected in conjunction with the M1 polarizing condition. This affected 21 transcripts in M1 cells, with 6 of them significantly upregulated in comparison to unpolarized macrophages, whereas 15 were downregulated. Slight changes in HSPs expression were observed in M2 cells when compared to unpolarized macrophages. Under these circumstances only five transcripts were significantly modulated. Interestingly, HSPBAP1 was the only HSP significantly downregulated in both M1 and M2 conditions parallel to a significant up-regulation of its target HSPB1. Conclusion: Our study revealed that monocytes undergoing maturation differentially regulate the expression of several members of HSPs and that distinct patterns of HSP expression characterize the M1 and M2 effector stages of macrophage life.
    Keywords: Heat shock proteins ; Monocytes/macrophages ; Differentiation
    ISSN: 1023-3830
    E-ISSN: 1420-908X
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  • 8
    Language: English
    In: Molecular Neurobiology, 2012, Vol.46(3), pp.605-613
    Description: Alzheimer's disease is the most common form of dementia among older people and is still untreatable. While β-amyloid protein is recognized as the disease determinant with a pivotal role in inducing neuronal loss and dementia, an impaired brain insulin signaling seems to account in part for the cognitive deficit associated with the disease. The origin of this defective signaling is uncertain. Accumulating toxic species of β-amyloid, the so-called oligomers, has been proposed to be responsible for downregulation of neuronal insulin receptors. We have found that the nontoxic form of β-amyloid, the monomer, is able to activate insulin/insulin-like growth factor-1 (IGF-1) receptor signaling and thus behaves as a neuroprotectant agent. Our suggestion is that depletion of β-amyloid monomers, occurring in the preclinical phase of Alzheimer's disease, might be the cause of early insulin/IGF-1 signaling disturbances that anticipate cognitive decline.
    Keywords: β-Amyloid ; Insulin ; Insulin-like growth factor 1 ; Alzheimer's disease
    ISSN: 0893-7648
    E-ISSN: 1559-1182
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  • 9
    Language: English
    In: Neurochemical Research, 2016, Vol.41(4), pp.924-932
    Description: mGlu1 and mGlu5 metabotropic glutamate receptors are expressed in the vertebrate retina, and are co-localized in some retinal neurons. It is believed that both receptors are coupled to polyphosphoinositide (PI) hydrolysis in the retina and their function may diverge in some cells because of a differential engagement of downstream signaling molecules. Here, we show that it is only the mGlu1 receptor that is coupled to PI hydrolysis in the retina. We used either bovine retinal slices or intact mouse retinas challenged with the mixed mGlu1/5 receptor agonist, DHPG. In both models, DHPG-stimulated PI hydrolysis was abrogated by the selective mGlu1 receptor antagonist, JNJ16259685, but was insensitive to the mGlu5 receptor antagonist, MPEP. In addition, the PI response to DHPG was unchanged in the retina of mGlu5 −/− mice but was abolished in the retina of crv4 mice lacking mGlu1 receptors. Stimulation of the mitogen-activated protein kinase pathway by DHPG in intact mouse retinas were also entirely mediated by mGlu1 receptors. Our data provide the first example of a tissue in which a biochemically detectable PI response is mediated by mGlu1, but not mGlu5, receptors. Hence, bovine retinal slices might be used as a model for the functional screening of mGlu1 receptor ligands. In addition, the mGlu1 receptor caters the potential as a drug target in the experimental treatment of degenerative disorders of the retina.
    Keywords: mGlu1 receptor ; Polyphosphoinositide hydrolysis ; Retina ; mice
    ISSN: 0364-3190
    E-ISSN: 1573-6903
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  • 10
    Language: English
    In: Cell and Tissue Research, 2012, Vol.347(1), pp.291-301
    Description: Alzheimer’s disease (AD) is a neurodegenerative disorder that affects about 35 million people worldwide. Current drugs for AD only treat the symptoms and do not interfere with the underlying pathogenic mechanisms of the disease. AD is characterized by the presence of β-amyloid (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Identification of the molecular determinants underlying Aβ-induced neurodegeneration is an essential step for the development of disease-modifying drugs. Recently, an impairment of the transforming growth factor-β1 (TGF-β1) signaling pathway has been demonstrated to be specific to the AD brain and, particularly, to the early phase of the disease. TGF-β1 is a neurotrophic factor responsible for the initiation and maintenance of neuronal differentiation and synaptic plasticity. The deficiency of TGF-β1 signaling is associated with Aβ pathology and neurofibrillary tangle formation in AD animal models. Reduced TGF-β1 signaling seems to contribute both to microglial activation and to ectopic cell-cycle re-activation in neurons, two events that contribute to neurodegeneration in the AD brain. The neuroprotective features of TGF-β1 indicate the advantage of rescuing TGF-β1 signaling as a means to slow down the neurodegenerative process in AD.
    Keywords: Alzheimer’s disease ; β-Amyloid ; Transforming growth factor-β1 ; Apoptosis ; Cell cycle activation ; Neuroprotection
    ISSN: 0302-766X
    E-ISSN: 1432-0878
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